Avian carcinoma virus MH2 contains two potential transforming genes, v-mht and v-myc. We have constructed deletion and frameshift mutants of each of the two genes by in vitro mutagenesis of cloned MH2 proviral DNA and tested their transforming function and virus production in cultured primary quail cells. We have found that the -myc gene transformed primary cells by itself without the second potential oncogene. v-mht was without detectable transforming function but may affect transformation by v-myc. We are currently investigating the possibility that v-mht may have an enhancing function of v-myc in animals. To study the dual oncogenes in another avian retrovirus, E26, we have constructed a replication-defective murine retrovirus carrying the v-myb and v-ets oncogenes derived from E26. The DNA construct, termed ME26, was transfected into NIH3T3 cells, together with pSV2neo, and G418-resistant colonies were selected. These cells were infected with a murine helper virus, and Northern analysis using aev-ets-specific probe indicated that the recombinant ME26 virus was present in the supernatant. The rescued virus could be successfully passed to NIH3T3 cells by infection. We have inserted a DNA segment containing 82% of the sor open reading frame of HTLV-III/LAV virus into a prokaryotic expression vector, pJL6. The bacterially-synthesized sor protein reacted with era from individuals infected with HTLV-III, indicating that sor was expressed as a protein product that was immunogenic in vivo. Antibodies to the purified, bacterially-synthesized sor protein immunoprecipitated a 23-kilodalton protein in HTLV-III-infected H9 cells, suggesting that this protein may be the sor gene product.